A5058620782- Cancer-related Molecular Pathways
- Signaling Pathways in Disease
- Ubiquitin and proteasome pathways
- Cell death mechanisms and regulation
- RNA modifications and cancer
- Epigenetics and DNA Methylation
- Hippo pathway signaling and YAP/TAZ
- RNA Research and Splicing
- Cancer Research and Treatments
- Peptidase Inhibition and Analysis
- MicroRNA in disease regulation
- Cancer Genomics and Diagnostics
- Cancer, Hypoxia, and Metabolism
- Toxin Mechanisms and Immunotoxins
- Nerve injury and regeneration
- Microtubule and mitosis dynamics
- DNA Repair Mechanisms
- Cancer Cells and Metastasis
- Genomics and Chromatin Dynamics
- Cancer-related gene regulation
- Retinoids in leukemia and cellular processes
- Endoplasmic Reticulum Stress and Disease
- Biochemical and Molecular Research
- Histone Deacetylase Inhibitors Research
- Protein Degradation and Inhibitors
IFOM
2007-2025
International Centre for Genetic Engineering and Biotechnology
1991-2025
University of Trieste
2015-2024
University of Naples Federico II
2023-2024
AREA Science Park
2013-2022
Weatherford College
2022
Consorzio Interuniversitario per le Biotecnologie
2008-2020
University of Trento
2018
Vitenparken
2013-2014
Instituto de Biología Molecular y Celular de Rosario
2011
The p27 mammalian cell cycle protein is an inhibitor of cyclin-dependent kinases. Both in vivo and vitro, was found to be degraded by the ubiquitin-proteasome pathway. human ubiquitin-conjugating enzymes Ubc2 Ubc3 were specifically involved ubiquitination p27. Compared with proliferating cells, quiescent cells exhibited a smaller amount ubiquitinating activity, which accounted for marked increase half-life measured these cells. Thus, abundance regulated degradation. specific proteolysis may...
The 66-kilodalton isoform of the growth factor adapter Shc (p66 ) translates oxidative damage into cell death by acting as reactive oxygen species (ROS) producer within mitochondria. However, signaling link between cellular stress and mitochondrial proapoptotic activity p66 was not known. We demonstrate that protein kinase C β, activated conditions in cell, induces phosphorylation triggers accumulation after it is recognized prolyl isomerase Pin1. Once imported, causes alterations Ca 2+...
Significance Accumulating evidence has underscored the role of cytosolic p53 in promoting cell death. Different reports have revealed that participates apoptosis induction by acting directly at mitochondria. However, because can mediate without its DNA-binding domain (the proposed to be fundamental for targeting mitochondria), mitochondrial localization is likely not only transcription-independent mechanism which promotes apoptosis. Here we demonstrate endoplasmic reticulum (ER) and...
Abstract Sterol regulatory element binding proteins (SREBPs) are a family of transcription factors that regulate lipid biosynthesis and adipogenesis by controlling the expression several enzymes required for cholesterol, fatty acid, triacylglycerol phospholipid synthesis. In vertebrates, SREBP activation is mainly controlled complex well-characterized feedback mechanism mediated crucial bio-product SREBP-activated mevalonate pathway. this work, we identified acto-myosin contractility...
Journal Article A one-tube plasmid DNA mini-preparation suitable for sequencing Get access Giannino Del Sal, Sal International Center Genetic Engineering and BiotechnologyPadriciano 99, 34012 Trieste, Italy Search other works by this author on: Oxford Academic PubMed Google Scholar Guidalberto Manfioletti, Manfioletti Claudio Schneider * To whom correspondence should be addressed Nucleic Acids Research, Volume 16, Issue 20, 25 October 1988, Page 9878, https://doi.org/10.1093/nar/16.20.9878...
A set of growth arrest-specific (gas) genes whose expression is negatively regulated by serum has recently been identified. We report on the detailed analysis one these (gas3). The kinetics regulation presence and absence were investigated, it was found that this gene at post-transcriptional level. encoded protein deduced from nucleotide sequence showed some similarity to a mitochondrial oxyreductase, in vitro translation established product transmembrane glycoprotein.
The p53 tumor suppressor gene is the most frequent target for genetic alterations in human cancers, whereas recently discovered homologues p73 and p63 are rarely mutated. We others have previously reported that tumor-derived mutants can engage a physical association with different isoforms of p73, inhibiting their transcriptional activity. Here, we report associate <i>in vitro</i> vivo</i> through respective core domains. show interaction mutant impairs sequence-specific DNA binding...
In response to DNA damage, p53 activates G(1)/S blocking and apoptotic genes through sequence-specific binding. also represses with no target site, such as those for Cdc2 cyclin B, key regulators of the G(2)/M transition. Like most promoters, they rely on multiple CCAAT boxes activated by NF-Y, whose binding is temporally regulated during cell cycle. NF-Y associates in vitro vivo alphaC helix NF-YC (a subunit NF-Y) a region close tetramerization domain p53. Chromatin immunoprecipitation...